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Journal of Dental Research
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*HomoloGene*UniGene
*Substance via MeSH
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*Cleft Lip and Palate
*Scars
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Biological

TGF-β3 Decreases Type I Collagen and Scarring after Labioplasty

R. Hosokawa1,*, K. Nonaka2,*, M. Morifuji3, L. Shum4 and M. Ohishi3,**

1 Graduate School of Dental Science,
2 Pediatric Dentistry, Division of Oral Health, Growth & Development, and
3 Division of Maxillofacial Diagnostic and Surgical Sciences, Faculty of Dental Science, Kyushu University, Maidashi 3-1-1, Higashi-ku, Fukuoka 812-8582, Japan; and
4 Cartilage Biology and Orthopaedics Branch, National Institutes of Health, Bethesda, MD, USA;

Correspondence: *corresponding author, m-ohishi{at}dent.kyushu-u.ac.jp

Cleft lip is a common congenital malformation, and labioplasty performed on infants to repair such defects often results in severe scar formation. Since TGF-β3 has been implicated in wound healing, we therefore hypothesized that TGF-β3 functions to reduce scarring after cleft lip repair. In this investigation, we demonstrated that exogenous TGF-β3 reduced scar formation in an incised and sutured mouse lip in vivo. During labioplasty, endogenous TGF-β3 expression was also elevated. In vitro experiments showed that exogenous TGF-β3 reduced type I collagen accumulation. Furthermore, TGF-β3 inhibited alpha-smooth-muscle actin expression, a marker for myofibroblasts. In tandem, TGF-β3 induced the expression and activity of MMP-9. Analysis of our data suggests that TGF-β3 is normally secreted following labioplastic wound healing. An elevated level of TGF-β3 reduces type I collagen deposition by restricting myofibroblast differentiation and thereby collagen synthesis, and by promoting collagen degradation by MMP-9. In combination, these events lead to TGF-β3-mediated reduced scar formation.

Key Words: cleft lip • CL/Fraser mouse • mesenchymal cells • myofibroblast • matrix metalloproteinase-9

Journal of Dental Research, Vol. 82, No. 7, 558-564 (2003)
DOI: 10.1177/154405910308200714
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